Electrocardiographic findings in a cross-sectional study of human immunodeficiency virus (HIV) patients in Enugu, south-east Nigeria

Njoku, Paschal; Ejim, EC; Anisiuba, BC; Ike, SO; Onwubere, Bjc

doi:10.5830/cvja-2016-007

Cited by 22 publications

(32 citation statements)

References 29 publications

(29 reference statements)

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“…The higher prevalence of QTc prolongation observed among HIV patients compared to healthy controls in our study has been variously reported by other researchers ( 12 , 22 – 25 ). Various reasons that account for this include autonomic dysfunction ( 25 ) and other established predisposing factors to QTc prolongation such as female sex, drugs and electrolyte abnormalities ( 26 ).…”

Section: Discussionsupporting

confidence: 86%

“…This is because the introduction of the Highly Active Anti-Retroviral Therapy (HAART) has significantly improved the survival of HIV patients and enabled them to live long enough to develop other systemic complications of the disease ( 3 ). Cardiovascular involvement in HIV/AIDS was recognized in the early days of the pandemic ( 4 ) and a wide spectrum of cardiovascular abnormalities ( 5 – 9 ) including electrocardiographic abnormalities such as corrected QT interval (QTc) prolongation ( 10 – 12 ) have been reported.…”

Section: Introductionmentioning

confidence: 99%

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The use of first line Highly Active Anti-Retroviral Therapy (HAART) is not associated with QTC prolongation in HIV patients

Ogunmodede

Kolo

Katibi

et al. 2017

Ethiop J Health Sci

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Background HAART has improved survival of HIV patients. Its contribution to the development of new cardiovascular abnormalities has generated much interest. This study aimed at determining the prevalence of QTc prolongation among HIV patients and determining the influence if any of the use of HAART on the QTc and on the risk of having QTc prolongation. Materials and Methods One hundred and fifty HIV positive subjects comprising 76 HIV positive subjects on HAART (Group A), 74 who were HAART- naïve (Group B), and 150 age and sex-matched healthy controls (Group C) were studied. All subjects had electrocardiography, and QTc duration was calculated. Results Mean QTc was significantly different among the three groups (P <0.001), highest in Group B > Group A > Group C. Frequency of QTc prolongation was highest in Group B (32%)>, Group A (17.3%)> Group C (4.7%) (P<0.001). Mean QTc was significantly longer among patients with CD4 count <200 cells/mm 3 than among those with >200 cells/mm 3 0.445 ± 0.03secs vs 0.421 ± 0.03secs (P<0.001). QTc prolongation was commoner among individuals with CD4 count <200 cells/mm 3 50% vs 20.5% (P<0.001). On binary logistic regression, none of the HAART medications used by our patients was predictive of the occurrence of QTc prolongation. Conclusion The QTc is longer, and QTc prolongation occurs more frequently in HAART-naïve HIV patients than patients on HAART and healthy controls. None of the HAART medications used by our patients was predictive of the development of QTc prolongation.

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Section: Discussionsupporting

confidence: 86%

Section: Introductionmentioning

confidence: 99%

The use of first line Highly Active Anti-Retroviral Therapy (HAART) is not associated with QTC prolongation in HIV patients

Ogunmodede

Kolo

Katibi

et al. 2017

Ethiop J Health Sci

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“…One of the possible explanations can be treatment with lopinavir (LPV) and zidovudine (ZVD) in seropositive patients. 31 Shavadia et al. noticed similar findings.…”

Section: Resultsmentioning

confidence: 69%

QT prolongation in HIV-positive patients: Review article

Liu

Shah

Basu‐Ray³

et al. 2019

Indian Heart Journal

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Introduction Antiretrovirals have immensely increased the average life expectancy of HIV-positive patients. However, the incidence of QT interval prolongation and other arrhythmias has also increased. Methods Pubmed and Google Scholar were searched for relevant literature published between 1990 and 2019. Results and discussion HIV-positive patients with high viral load, low CD4 count, chronic inflammation, and autonomic neuropathy can develop QT interval prolongation. Another factor prolonging QT interval includes exposure to the HIV transactivator protein, which inhibits hERG K (+) channels controlling IKr K (+) currents in cardiomyocytes. Protease inhibitors inhibiting the CYP3A4 enzyme can also lead to QT interval prolongation. QT interval prolongation can potentially be exacerbated by opioids, antipsychotics, antibiotics, and antifungals, the adjunct medications often used in HIV-positive patients. Hepatic insufficiency in seropositive patients on antiretrovirals may also increase the risk of QT interval prolongation. Conclusion Baseline and follow-up EKG in the susceptible population is suggested.

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“…Numerous studies have reported an increased prevalence of QT prolongation among HIV‐infected individuals compared to uninfected controls possibly due to concurrent administration of QT‐prolonging medications as well as the effect of the virus itself on the QTc interval 9‐12 . Table 1 summarizes six studies which compared the prevalence of QTc prolongation between HIV‐infected individuals vs. an uninfected control group 9,10,13‐16 . QT prolongation is a precursor for life‐threatening arrhythmias including torsades de pointes.…”

Section: Qt Prolongation/risk Of Torsades De Pointesmentioning

confidence: 99%

Sudden cardiac death in HIV‐infected patients: A contemporary review

Narla

2021

Clinical Cardiology

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HIV‐infected individuals have an increased risk of sudden cardiac death compared to the general population; yet the mechanisms underlying this increased risk remain unclear. The mechanisms underlying the heightened sudden cardiac death risk in HIV‐infected individuals is likely multifactorial. We reviewed the literature to elucidate and summarize the potential mechanisms contributing to sudden cardiac death in the HIV patient population. There is biologic plausibility that the following mechanisms may be contributing to the significantly heightened risk of sudden cardiac death in HIV to varying degrees: ventricular arrhythmias, myocardial fibrosis and scar, prolonged QTc interval (both as a direct effect of HIV on repolarization as well as a result of concurrent medications/antiretroviral therapies), substance abuse, structural heart disease, and premature atherosclerosis. Further understanding of the mechanisms underlying the increased sudden cardiac death risk in HIV can lead to identification of modifiable risk factors, implementation of public health programs, and potential revision of ICD implantation guidelines to ultimately reduce the incidence of sudden cardiac death in HIV‐infected patients. Further studies are needed to assess the relative contribution of each of these mechanisms and risk factors.

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Electrocardiographic findings in a cross-sectional study of human immunodeficiency virus (HIV) patients in Enugu, south-east Nigeria

Cited by 22 publications

References 29 publications

The use of first line Highly Active Anti-Retroviral Therapy (HAART) is not associated with QTC prolongation in HIV patients

The use of first line Highly Active Anti-Retroviral Therapy (HAART) is not associated with QTC prolongation in HIV patients

QT prolongation in HIV-positive patients: Review article

Sudden cardiac death in HIV‐infected patients: A contemporary review

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